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"Measles" derives from an Anglo-Saxon word implying it has been with us for a long time. The measles virus is a member of the Paramyoxidae, within the Morbillivirus genus and is one of the most contagious viruses to humans. The measles virus up until the 1960 was just a part of life, according to the National Immunization Program, 90% of people were infected with measles by age 15. During these times people who survived the virus in childhood grew an immunity too it (Rosaler, 2004.) In GB alone during 1940 - 1966 there was a reported half a million cases every epidemic year. Also between these times the deaths from Measles seemed to drop each year. (BMJ 1973)
The measles virus was first described in the 9th century by a Persian physician called Rhazes. The measles virus was first discovered in 1930's and further isolated in 1954 by a John F Enders. Following this Enders mentored a team of scientist who where responsible for the licensure of in the first live vaccine for measles in 1963. Nevertheless, the measles virus is still responsible for half a million deaths in 2004
(www.who.intâˆ•mediacentreâˆ•factsheetsâˆ•fs286âˆ•enâˆ•). This could be a result of a lack of health care support, objection to the vaccine and economical factors.
Infection and spread
The basic step of any infectious cycle is to gain entry into the host, survive and replicate within the host and to exit the host. The measles virus is no different. The measles virus spreads by aerosol droplets. According to Griffin and Oldstone an infected person will have a period of 10-14 days where the virus shows no symptoms followed by a few days of fever like symptoms and a rash.
These aerosol droplets act as vessels for the virus to travel from person to person and are extremely effective in spreading the disease. As these droplets are breathed in the virus travels to the epithelial cells of the respiratory tract. From here the virus travels to local lymph nodes from here the virus can enter the blood stream and travel into many organs including the lung, spleen, and finally the skin. The Measles virus replicates in epithelial and endothelial cells of these organs, the Measles virus can also replicate in monocytes, macrophages and T- cells. (Griffin and Oldstone, 2008)
This Replication within the lymphocytes causes lymphopenia, meaning the number of normal circulating lymphocytes is reduced. This allows the virus to spread through-out the body.
The measles virus can replicate in a wide range of cell types suggesting that these cell types all have something in common. In Order to infect a cell the Measles virus has to find a specific surface receptor. The first cell surface receptor identified was CD46 (Griffin and Bellini 1996). This surface cell receptor, CD46, is down regulated in when the cell becomes infected with the MV. Notably CD46 is not expressed in human erythrocytes and this lead to the discovery of another cell surface receptor CD150. CD150, also called SLAM (signalling lymphocytes activation molecule) is expressed on all immune cell and allows the MV virus entry into the cell. Their other cell surface receptors have not been discovered but allow for the entry into endothelial and epithelial cells. (Yanagi et al 2009)
As you can see from figure 1, by about day 12 is the peak of the infection and then it decreases drastically, this is due to the rapid increase of CD8+ T cells, show around 12-13 days following infection. This increase in T cell is due to the T cell mediated response that is mounted to control the measles virus. This T cell mediated response causes the associated rash as the T cells react with the antigen with the skin they also kill host epithelium skin cells. This reaction is said to be a hypertensive reaction. (www.humpath.com/measles).
The importance of this cell mediated immune response was highlighted by Permar et al 2003. He depleted CD8+ T cells in monkeys and infected the monkey with the wild-type measles virus. The animals depleted with CD8+ T cells displayed a more extensive rash, more measles being replicated at peak of infection and longer duration of viremia.
Antibodies first appear from 12-15 days from infection and the IgG antibody circulates in the blood for years and protect host from a further encounter with the Measles Virus.
Following the Measles Virus the Body is susceptible to secondary bacterial and viral infections such as diarrhoea and pneumonia. This is due to the associated immune suppression with the Meales virus. It has been shown that the innate and adaptive immune systems can be affected. In the adaptive immune system brief lymphopenia follows the Measles virus and poor proliferation of lymphocytes. Dendritic cells mature poorly and lose their ability to proliferate lymphocytes as shown on figure 2. (Kenrad E. Nelson 2006)
The time for the rash to develop from Measles is generally 2 weeks from infection, however, before the rash there is a prodromal stage lasting 2 - 3 days. These earlier symptoms are the running of the eyes (conjunctivas) and nose, cough and moderate fever. The break down of the epithelial cells in the lung due to the Measles virus results in an inflammatory reaction which causes these prodromal symptoms. (Zuckerman, 2009) also to note that the prodromal stage is the most infectious phase of the cycle.
The mucosal cells of the buccal cavity, adjacent to the molar teeth, are affected with the appearance of Koplik's spots forming. The Koplik spots are distinctive of the measles virus, which look like grains of salt beneath the mucosa and may be few or many in number.
Following the Koplik spots the rash will appear starting off in the face then spreading throughout for the next 2 days. The rash will appear to be a dull red and blotchy, these spots can be anything from 2-10 mm in diameter or merging into one another. Other manifestations of the Measles Virus include a sharp rise in body temperature to 40Â°C and diarrhoea in the early stages which indicates inflammatory lesions in the gut. (Collier, 1993.)
Vaccination is an attempt to make the body immune to a certain type of disease or infection. It has been possible to eradicate diseases such as small pox which was eradicated in 1979. An attempt to eradicate measles however has been as of yet unsuccessful.
Vaccination works by invoking an immune response by injecting a virus into the patient. The virus can be a live virus or a dead virus. The immune response in turn makes specific antibodies for the certain virus, in this case measles. These antibodies will be readily made by Memory B cells if the antigen is encountered again.
As I said in my introduction the measles virus was first discovered in 1930's and further isolated in 1954 by a John F Enders who in 1963 invented the first live vaccine for measles. The virus that Enders and his colleagues created was a live attenuated virus. An attenuated virus is a virus which is less virulent to humans. This attenuated virus is was a descendant of a viral strain isolated from a patient called David Edmonston.
In 1963 - 1975 the Edmonston B vaccine was available to the US and nearly 19 million doses of the vaccine was administered. (Preblud & Katz) The vaccine was stopped being used in 1975 because while the disease conveyed immunity to measles virus the side effects, such as a rash and a fever, were too common. An alternative vaccine replaced this one which has fewer side effects but equally effective. One of the vaccines that replaced Edmonston B vaccine was Moraten vaccine and is still used today in the US. (MMWR 1987). Mixed vaccines such as the MMR have been licensed and have the same effect at as the single strain vaccine. These vaccines vaccinate for measles, mumps and rubella.
The vaccine used to a single does of the vaccine at 15 months of ages. It was recommended by that in 1989 to increase it to a two dose vaccination. This recommendation was made by the American Academy of Paediatrics and some other organisations. The two dosage schedule was recommended because of an increase of young adolescents and adults catching the measles virus. The second does of vaccine should be administered between the ages of 4- 14 in patients. (AAP 2000).
Adverse effects from the vaccination occur in 5-15% develop fever and develop a high temperature. This reaction to the vaccine usually occurs between 5 to 11 days after vaccination. Another adverse effect of the vaccination to be noted is seizures that coincide with patients with fevers. While this is possible this complication is very rare and shouldn't deter people from the benefits of vaccination. (AAP 1987)
In 1998 there was a lot of controversy surrounding the MMR vaccine in the UK. It was surmised that the MMR vaccine was linked to Autism(Offit & Coffin 2003). This link was misinterpreted and further studies dismiss the claim that the MMR vaccine is linked with Autism. The most conclusive study was a study on half a million Danish children that found the relative risk of the MMR vaccine to be 0.92 for autism. (Madsen et al 2003)
Subacute sclerosing panencephalitis
Subacute Sclerosing Panencephalitis (SSPE) is a slow progressive disease which can be contracted after an acute measles virus infection. It is caused by persistent measles virus infecting the brain. (Hayashi et al 2002) SSPE is quite rare and occurs 1-10,000-30,000 patients (reviewed in Rima and Duprex 2005; Takasu et al. 2003) Patients usually affect with SSPE are children or young adults. However, more than 50 percent of cases result from patients who contracted measles when they where younger than 2.
With the early onset of SSPE patients will display changes in their mental status this will be followed by delirium, dementia, uncontrollable twitching, seizures, and eventually death. The clinical stages of SSPE were established by Jabbour et al (Jabbour 1969).
"1. Stage 1 manifests as cerebral changes and lasts 1 to 2 months.
2. Stage 2 involves worsening convulsions and lasts 2 to 3 months.
3. Patients in the Third Stage (coma and opisthotonus) exhibit worsening neurological status over 1 to 4 months.
4. The final stage of SSPE involves autonomic dysfunction and lasts months to years."
Biopsy's of the Brain in patients with SSPE have consistently reveal gray matter involvement, however white matter may be have extensive sclerosis. Neurons are predominantly affected; these affected neurons can have inclusions bodies in the nucleus or cytoplasm. (Horta-Barbosa et al1969). These inclusions have been shown to have the measles virus. Another feature of SSPE that differentiates from other CNS diseases is the elevated IgG antibody directed against measles antigens. (Baczko K et al 1988)
Figure 1 : Measles virus replication, clinical manifestations, and immune responses following infection. (Kenrad E. Nelson. 2006)
Figure 2. (Zuckerman, 2009.)